Author + information
- Received March 9, 1992
- Revision received April 24, 1992
- Accepted April 27, 1992
- Published online November 15, 1992.
- ↵∗Address for correspondence: Robert F. Rea, MD, Cardiovascular Division, Department of Medicine, University of Iowa, Iowa City, Iowa 52242.
Objectives. The purpose of the present study was to test the hypothesis that intravenous quinidine, unlike procainamide, causes direct vasodilation and reflexly mediated increases in sympathetic nerve activity.
Background. Intravenous quinidine can cause significant hypotension. Animal ejsprimente have suggested that quinidine blocks alpha-receptors and also refers vascular smootSi muscle by a nonadrenergic mechanism. In a recent study we showed that intravenous procainamide causes peripheral vasodilstion, hypotension and inhibition of sympathetic nerve activity in humans. Intraarterial procainamide, however, did not cause vasodilation.
Methods. Postganglionie muscle sympathetic nerve traffic was recorded from the peroneal nerve at the fibular head with tungsten microeiectrodes, and forearm blood flow was measured with venous occlusion plethysmography. Central venous pressure was measured directly. The direct effects of quinidine on vascular resistance were determined with brachial artery quinidine infusions and messurement of ipsilateral forearm blood flow.
Results. In eight normal subjects intravenous quinidine (8 mg/kg body weight infused for 27 min) decreased mean arterial pressure from 87 ± 3 (mean ± SE) to 83 ± 3 mm Hg, central venous pressure from 6.3 ± 0.6 to 5.0 ± 0.7 mm Hg and forearm vascular resistance from 32.2 ± 5.5 to 25.3 ± 4.7 U (all p < 0.05). Heart rate increased from 67 ± 4 to 77 ± 5 beats/min and muscle sympathetic nerve activity from 288 ± 70 to 660 ± 151 U/min (both p < 0.05). In five subjects intravenous nitroprusside that caused similar hemodynamic effects produced similar increases In sympathetic nerve activity. In eight subjects graded infusions of quinidine into the brachial artery (0.37, 0.74 and 1.48 mg/min) produced dose-dependent decreases in ipsilateral forearm vascular resistance and marked attenuation of forearm vasoconstriction caused by the cold pressor test.
Conclusions. These data show that quinidine, unlike procainamide, causes vasodilation directly and, when given intravenously, is associated with barorefles-mediated increases in sympathetic nerve activity.
↵1 Dr. Rea is a recipient of an American Heart Association Clinician-Scientist Award.
☆ This study was supported in part by a Grant-in-Aid from the American Heart Association, Dallas, Texas and Grant RR59 from the General Clinical Research Centers, Division of Research Resources, National Institutes of Health, Bethesda, Maryland.
- Received March 9, 1992.
- Revision received April 24, 1992.
- Accepted April 27, 1992.